This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The chronic lesions of inflammatory bowel disease (IBD) and Crohn's disease (CD) have many similarities to the chronic immunoinflammatory response in the oral cavity that destroys the soft and hard tissues of the periodontium (ie. periodontitis), potentially resulting in exfoliation of the teeth. While evaluation of the literature supports the common molecular components of the destructive inflammatory responses at the mucosal sites of these diseases, minimal data is available comparing/contrasting their characteristics in a common model system. Moreover, there is a burgeoning literature regarding dietary strategies for manipulation of IBD/CD, and other inflammatory diseases (eg. rheumatoid arthritis, psoriasis), these approaches are minimally developed with regard to adjunctive therapeutics for periodontal disease. Thus, we have developed 2 specific aims for this proposal that utilize a well defined animal model of mucosal inflammation and evaluate the impact of controlling reactive oxygen species (ROS) generated by the inflammation for ameliorating the disease symptoms. Specific Aim 1: To test the hypothesis that challenge of the periodontium with DSS or TNBS (agents that are known to elicit IBD in murine models) will stimulate periodontitis in these animals. Specific Aim 2: To test the hypothesis that treatment of mice with either Green tea polyphenols or 2-(RS)-n-propylthiazolidine-4(R)-carboxylic acid (PTCA), which target antioxidant pathways will ameliorate periodontitis induced by DSS and TNBS.